106 resultados para female entrepreneurship


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Knowledge spillover theory of entrepreneurship and the prevailing theory of economic growth treat opportunities as endogenous and generally focus on opportunity recognition by entrepreneurs. New knowledge created endogenously results in knowledge spillovers enabling inventors and entrepreneurs to commercialize it. This article discusses that knowledge spillover entrepreneurship depends not only on ordinary human capital, but more importantly also on creativity embodied in creative individuals and diverse urban environments that attract creative classes. This might result in self-selection of creative individuals into entrepreneurship or enable entrepreneurs to recognize creativity and commercialize it. This creativity theory of knowledge spillover entrepreneurship is tested utilizing data on European cities.

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While attributing urban success to more abundant supply of entrepreneurship, more recent studies on entrepreneurship have shifted their focus to examining cross-city variation in entrepreneurial activity. Despite a growing number of spatial-oriented studies of entrepreneurship worldwide to our best knowledge no empirical evidence exists on the determinants of cross-city variation in entrepreneurship in the context of the Former Soviet Union (FSU) states. Estrin and Mickiewicz (2010) show that transition economies generally exhibit lower rates of entrepreneurship than observed in most developed and developing market economies. This difference is even more pronounced for the FSU compared to Central and Eastern Europe. This paper investigates variation in entrepreneurial activity across FSU cities, attempting to bridge the city-level gap in spatial-oriented empirical research.

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In this chapter, I will focus on the female participation in what became known as ‘The Retomada do Cinema Brasileiro’, or the Brazilian Film Revival, by thinking beyond differences of gender, class, age and ethnicity. I will first re-consider the Retomada phenomenon against the backdrop of its historical time, so as to evaluate whether the production boom of the period translated into a creative peak, and, if so, how much of this carried onto the present day. I will then look at the female participation in this phenomenon not just in terms of numerical growth of women film directors, admittedly impressive, but only partially reflective of the drastic changes in the modes of production and address effected by the neoliberal policies introduced in the country in the mid 1990s. I will argue that the most decisive contribution brought about by the rise of women in Brazilian filmmaking has been the spread of team work and shared authorship, as opposed to a mere aspiration to the auteur pantheon, as determined by a notoriously male-oriented tradition. Granted, films focusing on female victimisation were rife during the Retomada period and persist to this day, and they have been, and continue to be, invaluable for the understanding of women’s struggles in the country. However, rather than resorting to feminist readings of representational strategies in these films, I will draw attention to other, presentational aesthetic experiments, open to the documentary contingent and the unpredictable real, which, I argue, suspend the pedagogical character of representational narratives. In order to demonstrate that new theoretical tools are needed to understand the gender powers at play in contemporary world cinema, I will, to conclude, analyse an excerpt of the film, Delicate Crime (Crime delicado, Beto Brant, 2006), where team work comes out as a particularly effective female, and feminist, procedure.

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Parents have large genetic and environmental influences on offspring’s cognition, behavior, and brain. These intergenerational effects are observed in mood disorders, with particularly robust association in depression between mothers and daughters. No studies have thus far examined the neural bases of these intergenerational effects in humans. Corticolimbic circuitry is known to be highly relevant in a wide range of processes including mood regulation and depression. These findings suggest that corticolimbic circuitry may also show matrilineal transmission patterns. We therefore examined human parent-offspring association in this neurocircuitry, and investigated the degree of association in gray matter volume between parent and offspring. We used voxel-wise correlation analysis in a total of 35 healthy families, consisting of parents and their biological offspring. We found positive associations of regional grey matter volume in the corticolimbic circuit including the amygdala, hippocampus, anterior cingulate cortex, and ventromedial prefrontal cortex between biological mothers and daughters. This association was significantly greater than mother-son, father-daughter, and father-son associations. The current study suggests that the corticolimbic circuitry, which has been implicated in mood regulation, shows a matrilineal specific transmission patterns. Our preliminary findings are consistent with what has been found behaviorally in depression, and may have clinical implications for disorders known to have dysfunction in mood regulation such as depression. Studies such as ours will likely bridge animal work examining gene expression in the brains and clinical symptom-based observations, and provide promising ways to investigate intergenerational transmission patterns in the human brain.

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We examine the black box of creativity, entrepreneurship and economic development by asking about the mechanisms through which creativity can influence economic development in cities. We propose that, like the knowledge spillover theory of entrepreneurship, creativity spillovers occur and can be slowed by a creativity filter. We examine how creativity and entrepreneurship, and creativity and a melting pot environment, interact to influence urban economic development. Using data on 187 cities in 15 European countries for the period 1999–2009, we advance the extant literature by providing evidence on the existence and dynamics of a creativity filter.

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The GPR30 is a novel estrogen receptor (ER) that is a candidate membrane ER based on its binding to 17beta estradiol and its rapid signaling properties such as activation of the extracellular-regulated kinase (ERK) pathway. Its distribution in the mouse limbic system predicts a role for this receptor in the estrogenic modulation of anxiety behaviors in the mouse. A previous study showed that chronic administration of a selective agonist to the GPR30 receptor, G-1, in the female rat can improve spatial memory, suggesting that GPR30 plays a role in hippocampal-dependent cognition. In this study, we investigated the effect of a similar chronic administration of G-1 on behaviors that denote anxiety in adult ovariectomized female mice, using the elevated plus maze (EPM) and the open field test as well as the activation of the ERK pathway in the hippocampus. Although estradiol benzoate had no effect on behaviors in the EPM or the open field, G-1 had an anxiolytic effect solely in the open field that was independent of ERK signaling in either the ventral or dorsal hippocampus. Such an anxiolytic effect may underlie the ability of G-1 to increase spatial memory, by acting on the hippocampus.

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BACKGROUND/AIMS: Estrogens are important effectors of reproduction and are critical for upregulating female reproductive behavior or lordosis in females. In addition to the importance of transcriptional regulation of genes by 17beta-estradiol-bound estrogen receptors (ER), extranuclear signal transduction cascades such as protein kinase A (PKA) are also important in regulating female sexual receptivity. GPR30 (G-protein coupled receptor 30), also known as GPER1, a putative membrane ER (mER), is a G protein-coupled receptor that binds 17beta-estradiol with an affinity that is similar to that possessed by the classical nuclear ER and activates both PKA and extracellular-regulated kinase signaling pathways. The high expression of GPR30 in the ventromedial hypothalamus, a region important for lordosis behavior as well as kinase cascades activated by this receptor, led us to hypothesize that GPR30 may regulate lordosis behavior in female rodents. METHOD: In this study, we investigated the ability of G-1, a selective agonist of GPR30, to regulate lordosis in the female mouse by administering this agent prior to progesterone in an estradiol-progesterone priming paradigm prior to testing with stud males. RESULTS: As expected, 17beta-estradiol benzoate (EB), but not sesame oil, increased lordosis behavior in female mice. G-1 also increased lordosis behavior in female mice and decreased the number of rejective responses towards male mice, similar to the effect of EB. The selective GPR30 antagonist G-15 blocked these effects. CONCLUSION: This study demonstrates that activation of the mER GPR30 stimulates social behavior in a rodent model in a manner similar to EB.

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The GPR30, a former orphan GPCR, is a putative membrane estrogen receptor that can activate rapid signaling pathways such as extracellular regulated kinase (ERK) in a variety of cells and may contribute to estrogen's effects in the central nervous system. The distribution of GPR30 in the limbic system predicts a role for this receptor in the regulation of learning and memory and anxiety by estrogens. Though acute G-1 treatment is reported to be anxiogenic in ovariectomised female mice and in gonadally intact male mice, the effect of GPR30 activation is unknown in gonadectomised male mice. In this study, we show that an acute administration of G-1 to gonadectomised male mice, but not female mice, was anxiolytic on an elevated plus maze task, without affecting locomotor activity. In addition, though G-1 treatment did not regulate ERK, it was associated with increased estrogen receptor (ER)alpha phosphorylation in the ventral, but not dorsal, hippocampus of males. In the female, G-1 increased the ERK activation solely in the dorsal hippocampus, independent of state anxiety. This is the first study to report an anxiolytic effect of GPR30 activation in male mice, in a rapid time frame that is commensurate with non-genomic signaling by estrogen.